We have some legitimate contenders in here. I'm g onna tell you in 15 minutes a quick overview of Trevi. Trevi, we have a single asset, nalbuphine ER. We are focused in difficult to treat chronic cough conditions. For those of you that have been following cough, it's been a difficult area. There's a huge unmet need. I think what we've brought to the space is a differentiated mechanism that not only works peripherally in the lung, but importantly centrally in the brain. We are the only investigational therapy that's had positive data in both idiopathic pulmonary fibrosis-related cough, but also refractory chronic cough. Two big conditions people have been working in. This is a specialty sales model. We are approaching it, you know, with a specialty focus that we can take this to market ourselves. It's got a big sales opportunity here. I'll take you through it, but it's about a $6 billion+ peak sales opportunity. Our mechanism, this is where it all starts. The drug works not only peripherally in the lung, it works along the spinal cord and the brainstem in the brain. That mediates coughing and breathing. This is the whole cough reflex arc, so being present in that whole pathway is helpful. To focus on our two lead indications of IPF and non-IPF. First of all, starting off with IPF. This is a terminal condition. It's about 140,000 patients in the U.S. You probably know there's been a lot of work done around antifibrotics, which essentially slow disease progression. We're focused on the patient, what upsets the patients' lives most drastically, and they talk about things like coughing, breathlessness, fatigue. Our drug is focused to lay alongside these antifibrotics and actually treat cough. We estimate that about 2/3 of those patients have uncontrolled coughing, so about 100,000 patients. This is terminal. They estimate about three to five years life expectancy and a big impact on these patients. If you focus on the right, this was a natural history database that was done on these patients, and it maps cough. You can see the top line, sort of more mild cough, moderate cough, severe cough, and it's mapped against the time to first hospitalization, death, or lung transplant. What the takeaway message from this is, the more severe your cough, it's more of an ominous outcome around this disease. Not surprising, you have progressive lung disease, and then you're adding on sort of coughing of 500 to 1,000 times a day on top of that. That creates a lot of inflammation, stretch fibers, et cetera, which exacerbate what's going on. There's been different drugs that have been tried in this space. It's been a tough nut to crack. What all those red dots represent is sort of those different slices or different mechanisms that have been tried. We came along, we had the first positive data readout in this space. The difference of sort of our drug, Haduvio, and what you see in all these other pie slices is those were peripherally acting only. They were working on one receptor in the lung. The problem is there's a lot of different triggers of cough. What's unique about our drug is not only do we work throughout the lung, but we'll catch cough coming up to the brain as well, and that's been the difference. I would also point out that antifibrotics have all studied cough and have not moved the needle there. They're essentially slowing disease progression, but cough is typically present at the beginning of the disease, and it stays present throughout the disease. Because you're not reversing disease here, the cough stays present throughout. Again, big unmet need that's not really served by the antifibrotics. We finished last year a phase II-B study, 160 patients. This was a six-week trial. It's a proper dose-ranging study. We looked at three different doses. The primary endpoint here is an objective cough monitor that counts the number of coughs. The key secondary is a cough severity scale. How much you cough is one thing, how severe that cough is another. We had lots of other endpoints as well that we looked at. This data all did get published in JAMA, you can go look at it. Just to summarize the efficacy data quickly on one slide, the upper left is the primary endpoint, the gray line is the placebo effect. The three different doses all statistically significant, you can see a dose response there. If you slide to the bottom left, this was the time course of this objective cough. We had a monitor on at baseline. We put one on at week two again, you can see the entire effect was there by the first time we measured it. The upper right is a responder analysis, we had pre-specified 30%, 50%, 75% reduction in cough. Again, big impact for these patients. If you just focus in the middle there, about 2/3 of these patients had their cough cut in half by the end of the six weeks. The bottom right's the one patient-reported outcome on this slide. It will be our key secondary in the next study. It's essentially the patient's assessment of cough severity. What you can see here is the green line is the 54 mg dose, and this was consistent across patient-reported outcomes that when you looked at it, the low dose just misses statistical significance, and the high dose didn't add a lot on the PROs. We ended up moving forward with the 54 mg dose. That's sort of a summary of the efficacy data. The other side of that coin, the adverse events, this has been a very predictable drug. It works, it works centrally in the brain, you're gonna see some of these different GI and CNS side effects, nausea, vomiting, dizziness, constipation. I think the hallmark here, if you focus on the bullets on the bottom, the placebo and the drug had similar discontinuation rates of about 5%- 5.5%. Not a big impact here for people staying on drug. 95% of these adverse events were mild to moderate, people were able to work through them. The SAEs were actually lower in the drug arm. I think the key of why people stayed on drug, if you focus on sort of the dose groups along the top, most of these AEs occur upon initiation of therapy, it's more about tolerability. We titrate this drug. We start low. As you can see here, as we were moving people up to the highest dose, adverse events are actually coming down. We have a separate graph we showed last week at our Investor Day that typically these AEs last anywhere from a couple of days to about nine or 10 days. As people work through the fir st week or two, they do just fine on the drug. Moving forward, we had a very constructive meeting with the FDA, our end of phase II meeting. We got very clear guidance out of the agency. We are running two studies, OCEAN 1, OCEAN 2. Essentially, we'll start off with our titration window. The first bigger study will go through 52 weeks of safety, so 54 weeks in total. I mentioned to you we're moving forward the 54 mg versus placebo. It's a two-to-one randomization, then we'll track patients three weeks off a drug. We also are gonna do a second confirmatory study. We only need to look at 12 weeks there. I should mention in the first study, the bigger study, the primary endpoint will be at 24 weeks. This is obviously answering the durability of effect question. The second study, OCEAN 2, will be a 12-week study. It's a little smaller. It's a couple of 100 patients. I'll show you in a minute why that is, why it's smaller than OCEAN 1. We'll start that study in the third quarter of this year. Just a timeline around this. OCEAN 1, we're starting this quarter. That'll run. It'll read out the first half of 2028. Although there's a 24-week efficacy endpoint, we're not unblinding the study till the end. OCEAN 2 is a 12-week study. We'll start in the third quarter. That'll read out second half of 2027. Think just some details on the bottom. You can see sort of roughly 80- 90 sites in the U.S., Canada, Spain, Poland, U.K. We're really focused on U.S. enrollment here. OCEAN 2, same thing, about 70- 80 sites. We are in the throes of things, of starting up all these sites and getting this study going. Primary endpoint's the same as what I just showed you. It's this change in baseline using the objective cough monitor. Two different time points I mentioned to you. On the right, this is important. We've actually powered in the bigger study all the way down through these eight secondary endpoints. There's a lot of things further down around breathlessness. We saw some good data, cough bouts, clinically meaningful changes. We're trying to, on the bigger study, really get all of that into the label. The second study is just confirming the primary and key secondary endpoint. We're also gonna add on to this. IPF is about half of the interstitial lung disease market. The other half consists of several different diseases, but what they have in common with IPF is they have lung fibrosis and they have cough. When you go in and add on that other piece of this grows to about 350,000 potential patients. From our perspective, it's really the same patient. They have a lot of comorbidities, RA, Sjögren's, you know, all kinds of different indications, but we're not treating the comorbidities. We're treating their cough and ILD. There's a tried and true path here from the antifibrotic work. Once you get IPF, you establish your dose, get that set up. You can do one trial in ILD, you can add it into your label. We're gonna go talk to FDA in the third quarter about that and look to initiate a study later this year. Refractory chronic cough, which is the third leg of the stool here. For those of you that don't know this disease, there's no FDA-approved therapies. There's been a lot of drugs tried here. It has a really high, high impact on the patient. Not surprising, I mean, on average, these people cough 1,000 times a day. A lot of anxiety, depression, impacts their work and non-work activities. Two in three women experience urinary incontinence. This tends to be about 2/3 of the patients are 50, 60-year-old women. This is another competitive landscape chart, and what it shows you is there's a lot of companies that have come and gone through here. You can see Bayer, Shionogi, GSK, Merck. A lot of people have had programs here. Again, back to peripheral-only agents. What's left in this space? GSK bought BELLUS, for any of you that followed that company a couple of years ago, for $2 billion. They'll read out their phase III data this quarter, third quarter of this year. We'll watch for that. I think they've had to migrate their program to only focusing on the most severe coughers. We think that we can have sort of a better option for patients here. There's another small company, Nocion, which will read out later this year as well with an inhaled therapy. Not a lot of competition here. We ran a two-way crossover study. This was about 60 patients, same primary endpoint, this objective measurement of cough. Similar secondary endpoints to what you saw. 21-day study. Just to summarize the data, you can see the upper left. There was a very big treatment effect in this condition. 65% reduction in cough after three weeks for these patients. That resulted in about a 56% treatment effect. The second-best set of data, which I know you can't cross-compare across trials, but in a trial that had been optimized by BELLUS Health, they had a 34% placebo-adjusted change. We've had much better data that's been shown to date. The bottom left answered an important question here because both Merck and GSK's program have had to migrate towards only looking at the most severe coughers. I think it's because they only affect cough being triggered through the P2X3 receptors. They're not touching anything else. In the coughs that they catch, they need to have a big effect. Because of our central mechanism, we had a hypothesis that it wouldn't matter for us what baseline cough counts here were. We stratified across people with 10-19 coughs an hour and greater than 20. What you can see here, if you focus on the blue bar, the drug arm, is it didn't matter what baseline cough counts were. This enabled us actually in our FDA discussions to have FDA encourage us to really open this up across cough counts. They don't want us focused on moderate and severe. If people have an issue with cough, they want them to be able to get our drug. Big effect. The bottom right's an interesting chart and sort of the jumping-off point for our next study, which is this was a titration study. People started at 27 mg, went to 54 mg, made their way up by the week three to 108 mg. What you can see here is we put a cough monitor on people after week one. That whole effect was there at the lowest dose at week one. Sort of in summary, big effect that worked in almost everyone across cough counts, and seems to work very rapidly at low doses. Adverse events, by the way, look the same. You see kinda the similar cast of characters here on the left. The bottom right chart sort of shows you what I mentioned before, which is most of these AEs happen in week one and then mitigate themselves over time. This is all about getting the titration schedule right. As we move forward, the question we need to answer in our phase II-B study is what is the minimally effective dose here? I think from that crossover trial, I'm not sure we know that. Remember, in IPF, our dose was 54 mgs BID. I just showed you in refractory chronic cough, it looks like the whole effect's there at 27 mg. We're going back. We're gonna run sort of a proper dose-ranging study. We'll look at 54 mgs BID, 27 mg BID, and we're actually looking at 27 mg QD to be given at night, most of this cough kicks off in the morning, to see if we can impact it with a much lower dose. This study is starting this quarter, and we'll also read out later in 2027, which I'll show you. Really kinda similar endpoints we already talked about. This is powered at 90% power, and we're excited to sorta see this next round of data. To wrap this up, our milestone chart. You can see we're kicking off both the refractory chronic cough and first IPF study this quarter. Then we'll start the second IPF cough-related trial and the non-IPF ILD IIb portion. We're actually doing one protocol. That'll roll into a phase III, assuming that goes well. What you can see here is this essentially results in a whole lot of data reading out in the second half of 2027, the final IPF trial reading out in the first half of 2028. If both of those are positive, we're planning for a second half of 2028 submission, so we're sort of eyeing that down. We do have, we had about $172 million at the end of the first quarter. We just did a nice offering here two weeks ago, so we have a little over $300 million on the balance sheet. That takes us through 2030, so that should get us through an approval on IPF. It gets us through our remaining development work on non-IPF ILD, and it'll get us through this study in RCC. What we have not funded here is a phase III in RCC or any of the commercial work. We can sort that out later. We feel like we're in good shape. We're in a space that has a big unmet medical need for patients. There's virtually very little competition left. We have the cash to execute against all these development milestones, and we'll not need to raise money off the back of all these. The company's well-positioned. That's Trevi. I will now take questions from the audience. Thank you for coming.